Angiotensin II, the principal effector of the renin-angiotensin cascade, stimulates a variety of physiological responses that support blood pressure and renal function. Abnormal generation of angiotensin II also contributes to the pathogenesis of hypertension, arterial diseases, cardiac hypertrophy, heart failure and proteinuric progressive renal diseases. It is well recognized that angiotensin-converting enzyme inhibitors effectively limit the progression of diabetic and non-diabetic proteinuric renal diseases towards end-stage renal disease, a capacity not necessarily shared by other blood pressure lowering agents. Whether angiotensin II type 1 receptor antagonists have the same renoprotective effect as angiotensin-converting enzyme inhibitors in progressive renal diseases remains ill defined. Angiotensin II type 1 receptor antagonists as antiproteinuric agents have been used originally in animal models of renal disease progression. Results have shown that angiotensin II type 1 receptor blockers are as effective as angiotensin-converting enzyme inhibitors in normalizing proteinuria in models of renal disease. Studies in humans are very few, but those that have been undertaken report consistent antiproteinuric effects of angiotensin II type 1 receptor antagonists that are similar to those with angiotensin-converting enzyme inhibitors. Long-term studies, however, are required to examine whether the antiproteinuric effects of angiotensin II type 1 receptor antagonists can be translated into renoprotection.
ASJC Scopus subject areas
- Internal Medicine